TABLE A-1
RECURRENCE RISKS GIVEN ONE SIBLING WHO HAS A CARDIOVASCULAR ANOMALY
|
Anomaly |
Suggested Risk (%) |
|
Ventricular septal defect |
3.0 |
|
Patent ductus arteriosus |
3.0 |
|
Atrial septal defect |
2.5 |
|
Tetralogy of Fallot |
2.5 |
|
Pulmonary stenosis |
2.0 |
|
Coarctation of the aorta |
2.0 |
|
Aortic stenosis |
2.0 |
|
Transposition of the great arteries |
1.5 |
|
Atrioventricular canal (complete endocardial cushion defect) |
2.0 |
|
Endocardial fibroelastosis |
4.0 |
|
Tricuspid atresia |
1.0 |
|
Ebstein’s anomaly |
1.0 |
|
Persistent truncus arteriosus |
1.0 |
|
Pulmonary atresia |
1.0 |
|
Hypoplastic left heart syndrome |
2.0 |
Modified from Nora JJ, Nora AH: The evaluation of specific genetic and environmental counseling in congenital heart diseases. Circulation 57:205-213, 1978.
TABLE A-2
AFFECTED OFFSPRING GIVEN ONE PARENT WITH A CONGENITAL HEART DEFECT
|
Defect |
Mother Affected (%) |
Father Affected (%) |
|
Aortic stenosis |
13.0–18.0 |
3.0 |
|
Atrial septal defect |
4.0–4.5 |
1.5 |
|
Atrioventricular canal (complete endocardial cushion defect) |
14.0 |
1.0 |
|
Coarctation of the aorta |
4.0 |
2.0 |
|
Patent ductus arteriosus |
3.5–4.0 |
2.5 |
|
Pulmonary stenosis |
4.0–6.5 |
2.0 |
|
Tetralogy of Fallot |
6.0–10.0 |
1.5 |
|
Ventricular septal defect |
6.0 |
2.0 |
From Nora JJ, Nora AH: Maternal transmission of congenital heart disease: New recurrence risk figures and the questions of cytoplasmic inheritance and vulnerability to teratogens. Am J Cardiol 59:459-463, 1987.
TABLE A-3
NEW YORK HEART ASSOCIATION FUNCTIONAL CLASSIFICATION∗
|
Class |
Impairment |
|
I |
The patient has the disease, but the condition is asymptomatic. |
|
II |
The patient experiences symptoms with moderate activity. |
|
III |
The patient has symptoms with mild activity. |
|
IV |
The patient’s condition is symptomatic at rest. |
∗ This is a classification of functional impairment in exercise capacity based on symptoms of dyspnea and fatigue. It is simple and useful in the evaluation of cardiac patients.
TABLE A-4
SUMMARY OF ANTIARRHYTHMIC AGENTS
AV, Atrioventricular; ECG, electrocardiogram.
TABLE A-5
EFFECTS OF ANTIARRHYTHMIC AGENTS ON THE ECG
Acu, Acute effect; Chr, chronic effect
Modified from Fischbach PS: Pharmacology of antiarrhythmic agents. In Macdonald Dick II (ed): Clinical Cardiac Electrophysiology in the Young. New York, Springer, 2010.
TABLE A-6
OXYGEN CONSUMPTION PER BODY SURFACE AREA∗
∗ In (mL/min)/m2.
From LaFarge CG, Miettinen OS: The estimation of oxygen consumption. Cardiovasc Res 4:23, 1970.
FIGURE A-1 Body surface area nomogram.
FIGURE A-2 Time course of elevation of selected serum markers after acute myocardial infarction in an adult. This figure summarizes the relative timing, rate of rise, peak values, and duration of elevation above the upper limit of normal for the serum markers. Myoglobin rises quickly soon after the onset of infarction but it is not specific for cardiac muscle; it may also come from skeletal muscles. Total creatine kinase (CK) rises within 4 to 8 hours, reaches a peak at 24 hours, and declines to normal levels within 2 to 3 days. There are three isoenzymes (BB, MM, and MB) of CK identified by electrophoresis. The CK-MB isoenzyme occurs primarily in cardiac muscles, the BB enzyme occurs primarily in the brain and kidneys, and the MM isoenzyme occurs in cardiac and skeletal muscles. Lactate dehydrogenase (LDH) elevation occurs several days after the onset of myocardial infarction. False elevation of LDH occurs in patients with hemolysis, leukemia, liver disease or congestion, renal disease, pulmonary embolism, skeletal muscle disease, shock, and myocarditis. Cardiac-specific troponin I may be useful for the diagnosis of infarction even 3 to 4 days after the event. In children, the normal value of cardiac troponin I has been reported to be 2 ng/mL or less, and it is frequently below the level of detection for the assay.(From Antman EM: General hospital management. In Julian DG, Barunwald E [eds]: Management of Acute Myocardial Infarction. London, WB Saunders, 1994, p 63.)
FIGURE A-3 Action potential of human ventricular myocyte of subepicardial origin.
• Phase 0 (rapid depolarization) is the results of sudden increase in membrane conductance to Na+ iron.
• Phase 1 (early rapid repolarization) is caused by transient outward K+ current.
• Phase 2 (plateau) is maintained by the competition between outward current carried by K+ and Cl- ions and inward current carried by Ca2+ ions.
• Phase 3 (final rapid repolarization) is caused by activation of repolarizing outward K+ current, and
• Phase 4 (the resting potential or diastolic depolarization) is caused by the Na-K pump that maintains high K+ concentration and low intracellular Na+ concentration by pumping K+ inward and Na+ outward.